The objectives of this research will be to determine whether or not there exists a physiological or pathological instance where the control of antidiuretic hormone (ADH) is influenced by the renin-angiotension system. This will be studied in the dog by removing the angiotensin II stimulation from the composite of inputs normally controlling ADH. This will be accomplished by the administration of angiotensin converting enzyme inhibitor during situations of physiologically and/or pathologically elevated plasma renin activity (PRA). PRA will be elevated by dehydration, low Na ion diet, and constriction of the renal artery. Studies will also be done to determine whether angiotensin II infusions similarly augment the osmotic stimulation of ADH release via hypothalamic and hepatic osmoreceptors in conscious dogs. Further studies on the role of aldosterone in the control of renin and ADH release will also be conducted in conscious and anesthetized dogs in order to document a direct negative feed back of aldosterone on renin release and its site of action.